This proposal deals with studies concerning the regulation of beta-glucosidase expression in the dimorphic fungus Mucor racemosus. This enzyme, whose appearance correlates with a specific developmental stage (mycelia), is regulated in a unique fashion. Cyclic adenosine monophosphate (cAMP) causes a reversible inactivation of beta-glucosidase. The inactivation both in vivo and in vitro is consistent with a mechanism involving a protein phosphorylation. I propose to perform experiments which will define the regulatory mechanism. These include isolation of the beta-glucosidase, performance of experiments which will determine whether the inactivation involves phosphorylation and characterization of that phosphorylation. In addition we will isolate and characterize regulatory mutants of beta-glucosidase and develop a genetic complementation system in order to do the characterization. This proposal is part of a long-range goal to define the regulatory role of cAMP in Mrcor development. Since both developmental processes and beta-glucosidase function in Mucor share a common regulatory element (cAMP), regulatory mutants of beta-glucosidase offer a high probability of being developmentally abnormal. Such mutants would lead to the establishment of cause and effect relationships between cAMP levels and morphogenesis.